Glucosamine sulfate was no better than placebo in reducing symptoms and progression of hip osteoarthritis. International Standard Randomised Controlled Trial Number: ISRCTN54513166.

The effects of GlcN on gene expression in a human osteoarthritic explant model suggest that enzymatic breakdown of the extra-cellular matrix might be reduced by the addition of 5mM GlcN. Additionally, restoration of already damaged cartilage is not to be expected, because gene expression of anabolic genes is also down-regulated. We suggest that chondroprotective properties of GlcN in vivo may be based on inhibiting further degradation due to catabolic activities, rather than on the ability to rebuild cartilage.

Because the most important evertor muscles are innervated by the fibular nerve, the significantly prolonged ACC-TIME of the affected ankle is consistent with the finding of a lower motor nerve conduction velocity of the fibular nerve after inversion trauma. The results support the concept of a delayed neuromuscular response as an important factor in the etiology of chronic ankle instability.

Background: Glucosamine (GlcN) used by patients with osteoarthritis was demonstrated to reduce pain, but the working mechanism is still not clear. Viscosupplementation with hyaluronic acid (HA) is also described to reduce pain in osteoarthritis. The synthesis of HA requires GlcN as one of its main building blocks. We therefore hypothesized that addition of GlcN might increase HA production by synovium tissue.

GS was not significantly better than placebo in reducing symptoms and progression of hip OA in subgroups of patients.